A dissociation of gamma-butyrolactone-induced absence seizure and CRE- and AP-1 DNA-binding activities in the developing rat brain.

Generalized absence epilepsy is a neurological childhood disorder which is characterized by behavioral arrest with staring and by 3 Hz spike and wave discharges (SWDs) in the electroencephalogram (EEG). In the present study, we investigated the correlation between behavioral and EEG changes and nuclear cAMP-responsive element (CRE)- and activator protein-1 (AP-1) DNA-binding activities during gamma-butyrolactone (GBL)-induced absence seizure in the developing rat brain. In the adult postnatal day 60 (P60) rat brain, both the transcription factor activation and absence seizure in behavior and EEG were simultaneously induced 15 min after GBL injection. In the infant P20 rat or young P40 rat, a higher sensitivity to GBL induced absence epilepsy in behavior and EEG 10-15 min after injection compared with that of adult rat. By contrast, no significant increase of CRE- and AP-1 DNA-binding activities could be seen in the infant thalamus. A significant increase in CRE- and AP-1 DNA-binding activities first occurred in the P30-40 young thalamus at 30 and 90 min, respectively, after GBL injection. Such a dissociation of high inducibility of behavior and EEG changes and low inducibility of CRE- and AP-1 DNA-binding activities in the infant or young rat clearly indicates that the activation of nuclear CRE- and AP-1 DNA-binding activities is a late occurring phenomenon with a different developmental maturation of thalamocortical circuit compared with absence seizure.